期刊
BIOLOGICAL PSYCHIATRY
卷 63, 期 4, 页码 377-384出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.biopsych.2007.06.012
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资金
- NCRR NIH HHS [K24 RR018192-02, K24 RR018192-04, K24 RR018192-05, K24 RR018192-01, K24 RR018192-03, K24 RR018192, K24 RR18192] Funding Source: Medline
- NIMH NIH HHS [R01 MH64821, R01 MH064821-01A2, R01 MH064821-03, R01 MH064821-02S1, R01 MH06603101, R01 MH064821, R01 MH064821-04, R01 MH064821-02] Funding Source: Medline
Background: Major depression is characterized by a negativity bias: an enhanced responsiveness to, and memory for, affectively negative stimuli. However, it is not yet clear whether this bias represents 1) impaired top-down cognitive control over affective responses, potentially linked to deficits in dorsolateral prefrontal cortex function; or 2) enhanced bottom-up responses to affectively laden stimuli that dysregulate cognitive control mechanisms, potentially linked to deficits in amygdala and anterior cingulate function. Methods: We used an attentional interference task using emotional distracters to test for top-down versus bottom-up dysfunction in the interaction of cognitive-control circuitry and emotion-processing circuitry. A total of 27 patients with major depression and 24 control participants was tested. Event-related functional magnetic resonance imaging was carried out as participants directly attended to, or attempted to ignore, fear-related stimuli. Results: Compared with control subjects, patients with depression showed an enhanced amygdala response to unattended fear-related stimuli (relative to unattended neutral). By contrast, control participants showed increased activity in right dorsolateral prefrontal cortex (Brodmann areas 46/9) when ignoring fear stimuli (relative to neutral), which the patients with depression did not show. In addition, the depressed participants failed to show evidence of error-related cognitive adjustments (increased activity in bilateral dorsolateral prefrontal cortex on posterror trials), but the control group did show them. Conclusions: These results suggest multiple sources of dysregulation in emotional and cognitive control circuitry in depression, implicating both top-down and bottom-up dysfunction.
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